Pathophysiology of hypertension in the absence of nitric oxide/cyclic GMP signaling.

Abstract

The nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) signaling system is a well-characterized modulator of cardiovascular function, in general, and blood pressure, in particular. The availability of mice mutant for key enzymes in the NO-cGMP signaling system facilitated the identification of interactions with other blood pressure modifying pathways (e.g. the renin-angiotensin-aldosterone system) and of gender-specific effects of impaired NO-cGMP signaling. In addition, recent genome-wide association studies identified blood pressure-modifying genetic variants in genes that modulate NO and cGMP levels. Together, these findings have advanced our understanding of how NO-cGMP signaling regulates blood pressure. In this review, we will summarize the results obtained in mice with disrupted NO-cGMP signaling and highlight the relevance of this pathway as a potential therapeutic target for the treatment of hypertension.

• Authors: Robrecht Thoonen, Patrick Y Sips, Kenneth D Bloch, Emmanuel S Buys
• Journal: Current hypertension reports (Curr Hypertens Rep) Vol. 15 Issue 1 Pg. 47-58 (Feb 2013) ISSN: 1534-3111 [Electronic] United States
• PMID: 23233080 (Publication Type: Journal Article)

Chemical References

• Nitric Oxide
• Cyclic GMP-Dependent Protein Kinases
• Cyclic GMP

Topics

• Animals
• Blood Pressure (physiology)
• Cyclic GMP (metabolism, physiology)
• Cyclic GMP-Dependent Protein Kinases (metabolism)
• Endothelium, Vascular (physiology)
• Genome-Wide Association Study
• Humans
• Hypertension (physiopathology)
• Mice
• Mice, Mutant Strains
• Models, Animal
• Nitric Oxide (metabolism, physiology)
• Signal Transduction (physiology)
• Vasoconstriction (physiology)
• Vasodilation (physiology)